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The prenatal influence of rubella on development

发布时间:2017-04-04
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The nature of prenatal development was once thought to depend solely on an individual's genes. However, nowadays it is generally accepted that environmental influences can act upon an unborn child to cause a range of physical and behavioural effects. Some environmental influences, such as good nutrition, help to enrich development. However, harmful substances known as teratogens can often impact upon an unborn child to cause abnormalities in development. The first teratogen to be identified was rubella, which can cause Congenital Rubella Syndrome (CRS) in babies if their mothers contract the illness whilst pregnant. Evidence has shown that prenatal exposure to rubella is linked to physical defects, and to behavioural issues including autism and schizophrenia. This occurs because small microorganisms, like the rubella virus, are able to pass through the placenta to infect the unborn child (Whitley & Stagno 1991). Therefore, it may be incorrect to assume that factors acting on the unborn child are not important for development.

Moore and Persaud (1993) stated that each organ system is most vulnerable to disruption by environmental influences when it is developing most rapidly. This is likely to be in the second stage of development, the embryonic stage, which starts in the third week of pregnancy and lasts until sixteenth week. This stage signals the development of the fetus's organs and limbs, and they rapidly develop in this time. The unborn child is sometimes susceptible during the fetal stage as well, during the process of organ refinement. Therefore, there are various critical periods for the developing fetus whereby rubella infection may have a detrimental effect on development. These effects of prenatal rubella were first observed by Gregg (1941). Following an epidemic of Rubella in Australia, Gregg noted that women who had contracted the disease whilst pregnant often gave birth to babies who had eye cataracts. Gregg's discovery spawned interest into the subject, and further research aimed to examine whether there were any other physical or mental consequences of maternal rubella infection.

The physical implications of prenatal rubella are extensive, including eye diseases and hearing loss, which are apparent at birth. Eye diseases have been noted in 78% of babies born to mothers who were infected with rubella in the first trimester of pregnancy (Givens, Lee, Jones, & Ilstrup, 1993). Congenital rubella affects almost all eye structures (Vijayalakshmi, Kakkar, Samprathi, & Banushree, 2002), and can result in blindness due to congenital cataracts, glaucoma, or several other diseases. Exposure to rubella can also cause hearing loss or deafness in babies; research conducted by Parving, Vejtorp, Møller, and Hartvig Jensen (1980) found that 63% of congenitally deaf children tested positive for the rubella antibody, suggesting that their bodies had been prenatally infected with rubella. The conclusion can be drawn, therefore, that the environmental influence of rubella can negatively affect the physical development of an unborn child.

Whilst most fetal organs are only vulnerable to environmental influences for a short length of time, the brain undergoes rapid development throughout most of the pregnancy (Moore & Persaud), which heightens its' susceptibility to teratogens. Viruses such as rubella are one of the most common causes of mental disturbances and brain dysfunction (Brown & Susser, 1999). Many studies have made attempts to explain the neuropathological mechanisms by which prenatal rubella exposure can impact upon the brain. A study conducted by Plotkin, Dudgeon and Ramsay (1963) found that when human cells were infected with the rubella virus, they exhibited slower growth and reduced doubling capacity. The rubella virus acts to inhibit mitosis which consequently leads to poor prenatal brain development (South & Sever, 1985). It may be via these prenatal mechanisms that developmental disorders, such as autism or schizophrenia, have the capacity to develop.

One behavioural disorder which has been recognised in children with CRS is that of autism, which is frequently accompanied by mental retardation. McIntosh and Menser (1992) reported that 42% of those diagnosed with CRS experience mental retardation, which is severe and often permanent. Due to the association between mental retardation and childhood autism, studies have assessed the degree to which congenital rubella may be a contributing factor in the development of autism. In her study into the behaviour of children with CRS, Chess (1971) observed 10 children out of 243 who had autism. Chess therefore stated that the prevalence of autism amongst children with CRS is 412 per 10,000; this is a stark contrast to the general population statistics, where between 5 and 13 children out of 10,000 develop autism (Fombonne, 2005). This shows that the autism in those with CRS was not just chance occurrence, and that their autism was directly related to rubella exposure. In a review of all the available evidence, Landrigan (2010) postulates that autism has a genetic basis, but that early environmental influences during pregnancy also contribute to its development. Landrigan claims that the strongest evidence for the causes of autism comes from those studies which link it to early environmental influences, including maternal rubella infection. Therefore, from the research into autism, it is fairly clear that prenatal factors can and do impact upon the unborn child to influence development.

Not only can CRS contribute to the development of autism, but prenatal exposure to rubella is also linked to increased risk of schizophrenia in later life. The 'Neurodevelopmental hypothesis of schizophrenia' (Waddington et al., 1999) suggests that disruption to the brain during its' developmental period, for example by rubella, creates a vulnerability to psychiatric illnesses like schizophrenia later in life. The results of a study by Brown et al., (2001) support this view; at the age of 21-23, those individuals who had been prenatally exposed to rubella were significantly more likely to be suffering from schizophrenia than the non-exposed comparison sample. Further evidence for the link comes from Lim et al. (1995), who found that schizophrenic patients with a history of congenital rubella had significantly reduced brain volume compared to schizophrenic patients or control patients. This suggests that prenatal rubella inhibits the brain from growing to its full size, and hence this offers indirect support for the neurodevelopmental hypothesis. Further imaging studies of schizophrenic patients have also shown abnormalities in the brain which are consistent with the neuronal loss typically seen in those with CRS (Beasley and Reynolds 1997). Therefore, it may be that when rubella infection causes cell loss and lack of growth in the brain of the unborn child, it impacts on the areas of the brain which are associated with schizophrenia risk. These findings regarding schizophrenia add weight to the view that factors acting upon the unborn child are vitally important for development.

Despite these significant findings into autism and schizophrenia, there are some limitations to the research which need to be considered. The biological processes of fetal infection by rubella may be complicated by confounding factors. The incidence of rubella in the developed world has decreased with the introduction of the Measles, Mumps, and Rubella (MMR) vaccination, yet for developing countries the vaccination may not be available. This means that a baby born with CRS is likely to be born into a developing country, where it was not possible to vaccinate the mother against such a risk. Therefore, the effects of rubella on later psychiatric manifestations such as schizophrenia are likely to be complicated by other factors related to deprivation. For example, the child may also have experienced prenatal malnutrition, and this is a factor which has been linked to increased schizophrenia risk (Susser & Lin, 1992). Therefore, the schizophrenia may be related to malnutrition rather than rubella infection. The diagnosis of psychological problems may also be confounded by the physical manifestations of CRS. In children who are congenitally blind without CRS, a higher incidence of autism has been found, and this has been linked to the children's deprivation of perceptual experience (Brown, Hobson, Lee, & Stevenson, 1997). Therefore, in those children who are born with congenital blindness, and who also have CRS, it may be the blindness that is linked to the development of autism rather than the rubella infection. A final limitation of the research into rubella is that much of it is becoming outdated; research was mostly conducted following the rubella epidemics which broke out in the 1940's, and the 1960's. Due to these weaknesses, Thapar and Rutter (2009) state that research into prenatal influences and developmental outcomes should be approached with caution.

In conclusion, it is widely accepted that rubella has causal effects on physical development. Numerous studies have also shown that exposure to rubella can also impact upon the unborn child to increase his or her susceptibility to autism or schizophrenia. As conclusive as the research might be, these claims should be carefully considered before they are accepted, as there are some factors which could complicate the study of rubella on developmental outcomes. Nevertheless, there are clearly some effects of rubella upon the fetus, both physically and mentally. Therefore, it can be concluded that factors acting upon the unborn child are indeed important for development.

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